Take a deep breath and wake up: The protean role of serotonin preventing sudden death in infancy

Cummings, Kevin J.; Leiter, James C.

doi:10.1016/j.expneurol.2019.113165

Cited by 8 publications

(2 citation statements)

References 136 publications

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“…Dysfunctional serotoninergic neurotransmission has a pivotal role in the pathogenesis of SIDS [55]. Serotonin is crucial for the recovery from hypoxic reflex apnea including gasping, restoration of heart rate and blood pressure, termination of apnea and, ultimately, restoration of eupnea and arousal [56 ▪ ]. In a potentially analogous pathophysiological process, impaired serotonergic neurotransmission may play a role in SUDEP [57 ▪ ].…”

Section: Serotonergic Pathways and Their Role In Sudden Deathmentioning

confidence: 99%

Sudden unexpected death in children: myth or reality?

Enner

Pavkovic

Kothare

2021

Current Opinion in Pediatrics

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Purpose of review Despite many years of study, sudden unexplained death remains a tenuous diagnosis of exclusion. Here, we discuss the current science behind the uncertainties of sudden death, as well as the questions that still remain. Recent findings Failure in any part of the complex interplay between peripheral sensors and central cardiorespiratory regulation can result in sudden death. Diagnostic testing with electrocardiograms, electroencephalogram, sleep studies, or even genetic studies have increased our ability to identify patients at the highest risk. Summary Advances in the understanding of sudden unexplained death in children may show common pathways leading to sudden death from multiple different diseases. Although rare, the devastating implication prioritizes the importance in educating patients about how to live with the risk of sudden death.

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Section: Serotonergic Pathways and Their Role In Sudden Deathmentioning

confidence: 99%

Sudden unexpected death in children: myth or reality?

Enner

Pavkovic

Kothare

2021

Current Opinion in Pediatrics

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“…Carotid chemoreceptors operate through multiple paths in the raphe-pontomedullary respiratory network with its embedded, dynamically configured memory system regulated by serotonin (5-hydroxytryptamine, 5-HT) (4). Enhanced brainstem release of 5-HT follows the onset of severe hypoxia (15,16), and many studies have implicated brain stem deficiencies in serotonin as a contributing factor in sudden infant death syndrome (SIDS) (17)(18)(19). SIDS is associated with evidence of hypoxia and failed autoresuscitation (20)(21)(22)(23).…”

Section: Introductionmentioning

confidence: 99%

Hypoxia evokes a sequence of raphe-pontomedullary network operations for inspiratory drive amplification and gasping

Nuding,

Segers,

Iceman

et al. 2023

Preprint

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Hypoxia can trigger a sequence of breathing-related behaviors, from tachypnea to apneusis to apnea and gasping, an autoresuscitative behavior that, via large tidal volumes and altered intrathoracic pressure, can enhance coronary perfusion, carotid blood flow, and sympathetic activity, and thereby coordinate cardiac and respiratory functions. We tested the hypothesis that hypoxia-evoked gasps are amplified through a disinhibitory microcircuit within the inspiratory neuron chain and a distributed efference copy mechanism that generates coordinated gasp-like discharges concurrently in other circuits of the raphe-pontomedullary respiratory network. Data were obtained from 6 decerebrate, vagotomized, neuromuscularly-blocked, and artificially ventilated adult cats. Arterial blood pressure, phrenic nerve activity, end-tidal CO2, and other parameters were monitored. Hypoxia was produced by ventilation with a gas mixture of 5% O2in nitrogen (N2). Neuron spike trains were recorded at multiple pontomedullary sites simultaneously and evaluated for firing rate modulations and short-time scale correlations indicative of functional connectivity. Experimental perturbations evoked reconfiguration of raphe-pontomedullary circuits during tachypnea, apneusis and augmented bursts, apnea, and gasping. The functional connectivity, altered firing rates, efference copy of gasp drive, and coordinated step increments in blood pressure reported here support a distributed brain stem network model for amplification and broadcasting of inspiratory drive during autoresuscitative gasping that begins with a reduction in inhibition by expiratory neurons and an initial loss of inspiratory drive during hypoxic apnea.

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